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EGR3 通过上调 MYC 和 CDK1 促进胶质母细胞瘤细胞生长。

EGR3 Promotes Glioblastoma Cell Growth with Upregulation of MYC and CDK1.

作者信息

Chang Chia-Wei, Chou Yi-Chin, Huang Yin-Cheng, Cheng Yi-Chuan

机构信息

Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan.

Department of Neurosurgery, Chang Gung Memorial Hospital at Linkou Medical Center, Taoyuan 333423, Taiwan.

出版信息

Int J Mol Sci. 2025 Jun 20;26(13):5931. doi: 10.3390/ijms26135931.

Abstract

Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, characterized by rapid growth and resistance to therapy. Despite extensive research, the molecular mechanisms driving GBM progression remain incompletely understood. In this study, we employed integrative transcriptomic analysis to identify transcription factors associated with GBM, revealing EGR3 as a key candidate. Functional assays demonstrated that EGR3 promotes GBM cell viability, with EGR3 overexpression significantly enhancing cell growth, while EGR3 disruption impaired viability. To elucidate the downstream targets of EGR3, we further performed transcriptomic analysis and identified and as significantly upregulated in response to EGR3 overexpression. These results suggest that EGR3 is associated with enhanced GBM cell growth, potentially through the regulation of and . Our findings provide a clear model linking EGR3 to GBM proliferation and highlight MYC and CDK1 as potential therapeutic targets. This study advances the understanding of transcription factor-associated oncogenesis in GBM and suggests that targeting EGR3 may offer a novel therapeutic strategy.

摘要

胶质母细胞瘤(GBM)是最具侵袭性和致命性的原发性脑肿瘤,其特征是生长迅速且对治疗具有抗性。尽管进行了广泛研究,但驱动GBM进展的分子机制仍未完全了解。在本研究中,我们采用综合转录组分析来鉴定与GBM相关的转录因子,发现EGR3是关键候选因子。功能分析表明,EGR3促进GBM细胞活力,EGR3过表达显著增强细胞生长,而EGR3缺失则损害细胞活力。为了阐明EGR3的下游靶点,我们进一步进行转录组分析,并确定[此处原文缺失具体基因名称]在EGR3过表达时显著上调。这些结果表明,EGR3可能通过调节[此处原文缺失具体基因名称]与增强GBM细胞生长相关。我们的研究结果提供了一个将EGR3与GBM增殖联系起来的清晰模型,并突出了MYC和CDK1作为潜在治疗靶点。本研究推进了对GBM中转录因子相关肿瘤发生的理解,并表明靶向EGR3可能提供一种新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/245a/12249872/43f384d6532f/ijms-26-05931-g001.jpg

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